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acute respiratory tract infection
Acute respiratory infections (ARI) are responsible for 20% of childhood deaths under 5 years of age, with pneumonia accounting for 90% of ARI mortality. Children under 2 years old, malnourished children, children with HIV, and those with poor access to healthcare or poorly educated parents are most at risk. ARIs are a common cause of outpatient visits (20-60%) and admissions (12-45%) in children. Common respiratory infections affecting children include the common cold, acute epiglottitis, croup, ear infections, tonsillitis, sinusitis, and pneumonia. Bacteria and viruses can cause ARIs, with symptoms and severity depending on the specific infectious agent.
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acute respiratory tract infection
- 1. DR Anwar ahmad COMMUNITYMEDICINE & PUBLIC HEALTH KGMU UP LUCKNOW
- 2. Problem statement ŠARI RESPONSIBLE FOR 20% OF CHILDHOOD (< 5 YEARS) DEATHS (IN WHICH 90% FROM PNEUMONIA) Š ARI MORTALITY HIGHEST IN CHILDREN- HIV-infected Under 2 year of age Malnourished Weaned early Poorly educated parents Difficult access to healthcare Š OUT- PATIENT VISITS 20-60% Š ADMISSIONS 12-45%
- 3. Children with ARIpresenting in OPD Place % of children London (UK) 35.0 Herston (Australia) 34 Ethiopia (Whole country) 25.5 Sau aulo (Brazil) 41.8 India 38.9 Nepal 37.6
- 4. Varied agents– Bacteria and viruses Clinical picture may vary with etiological agent May be present in normal people but may cause disease in only few. Epidemiology
- 5. Infections of therespiratory tract are described in a number of different ways according to the general areas of involvement in the more common infections. The upper respiratory tract or upper airway consists of primarily of the nose and pharynx. The lower respiratory tract consists of bronchi and bronchioles, which constitute the reactive protein of the airway because of their smooth muscle content and ability to constrict the alveoli. ACUTE RESPIRATORY INFECTIONS
- 6. May causethe inflammation of respiratory tract anywhere from nose to alveoli. May be classified as – AURI – Acute Upper Respiratory Infection (common cold, pharyngitis, epiglottitis, & otitis media etc.) or ALRI – Acute Lower Respiratory Infection (laryngitis, layngotracheitis, bronchitis, bronchiolitis & pneumonia) ACUTE RESPIRATORY INFECTIONS(ARI)
- 7. Anatomy of theRespiratory system
- 8. AGENT FACTORS BACTERIA AGEGROUP AFFECTED CHRACTERISTIC CLINICAL FEATURES Bordetella pertussis Infants & young children Poroxysmal cough Corynebacterium diphtheriae Children diphtheria Hemophilus influenzae Adults Children Acute ex of ch bronchitis Acute epiglottitis Klebsiella pneumoniae Adults Lobar pneumonia Legionella pneumophila Adults Pneumonia Staph. pyogenes All ages Lobar and bronchopneumonia Strep. pneumoniae All ages Pneumonia Strep. pyogenes All ages Acute pharyngitis and tonsillitis
- 9. VIRUSES AGE GROUP AFFECTED CHRACTERISTIC CLINICALFEATURES Enterovirus All ages Febrile pharyngitis Influenza A, B, C All ages variable Measles Young children variable Parainfluenza 1, 2, 3 Young children variable Respiratory Syncytial Virus Infants and young children Severe bronchiolitis and pneumonia Rhinovirus All ages Common cold Coronavirus All ages Common cold AGENT FACTORS
- 10. Factors Affecting Typeof Illness and Physical Response in Acute Respiratory Infections:
- 11. Nature of infectiousagent: The respiratory tract is subjected to a wide variety of infectious agents. Size and frequency of dose: The larger the dose and the more frequent the exposure, the greater the likelihood of a significant infection. Age of child: Children of preschool and school age are more often exposed to infectious agents generally after 3 months of age infants have less resistance to infections. Size of child: Airways are smaller in young children and more subjected to considerable narrowing from edema.
- 12. Ability to resistinvading organisms: School age children have greater resistance to infection than infants and young children. Presence of great conditions: Malnutrition, anemia, fatigue, chilling of the body and immune deficiencies decrease normal resistance to infection. Presence of disorders affecting respiratory tract: Allergies, cardiac abnormalities and cystic fibrosis weaken respiratory defense mechanism. Seasons: The most common respiratory tract pathogens appear in epidemics during winter and spring months.
- 13. RHINITIS (COMMONCOLD OR CORYZA) RHINOVIRUSES, ENTEROVIRUSES, CORONAVIRUSES ACUTE EPIGLOTTITIS (SUPRGLOTTITIS) CROUP (ACUTE LARYNGOTRACHEOBRONCHITIS) EAR INFECTIONS (ACUTE OTITIS MEDIA) VIRUSES, PNEUMOCOCCUS, GABHS, HEMOPHILUS INFLUENZA, MORAXELLA CATARRHALIS ACUTE INFECTIOUS LARYNGITIS VIRAL/DIPTHERIA ACUTE PHARYNGITIS ADENOVIRUS, ENTEROVIRUS, RHINOVIRUS, GROUP A BETA HEMOOLYTIC STREPTOCOCCUS(older children) TONSILLITIS GROUP A BETA HEMOLYTIC STREPTOCOCCI, EBV SINUSITIS VIRAL/BACTERIAL UPPER RESPIRATORY TRACT INFECTIONS
- 14. Children average8 episodes per year, adults 3 episodes per year Etiologies : Rhinoviruses 30 to 35% Coronaviruses about 10% Miscellaneous known viruses about 20% Influenza and adenovirus-30% Presumed undiscovered viruses up to 35% Group A streptococci 5% to 10% Parainfluenza was the first respiratory virus isolated (1955) Seasonal variation Rhinovirus early fall Coronavirus- winter The Common Cold
- 15. Common symptoms aresore throat, runny nose, nasal congestion, sneezing, Sometimes accompanied by conjunctivitis, myalgias, fatigue Sinusitis often present by CT scan; “rhinosinusitis” might be a better term Common Cold
- 16.
- 17. Direct contactis the most efficient means of transmission: 40% to 90% recovery from hands. Infectious droplet nuclei Brief exposure (e.g., handshake) transmits in less than 10% of instances Kissing does not seem to be a common mode of transmission. Transmission of rhinoviruses
- 18. Incubation period12-72 hours Nasal obstruction, drainage, sneezing, scratchy throat Median duration 1 week but 25% can last 2 weeks Pharyngeal erythema is commoner with adenovirus than with rhino or coronavirus Clinical characteristics
- 19. Main challengeis to distinguish between uncomplicated cold and streptococcal pharyngitis or bacterial sinusitis Good examination Marked exudate or pharyngeal erythema suggests Streptococcal infection Adenovirus Diphtheria Rapid antigen tests for group A streptococcus Rapid techniques for influenza, RSV, parainfluenza Treat with NSAIDs and whatever else your grandmother advises Diagnosis and treatment
- 20. Life-threatning infectionof the epiglottis, the aryepiglottic folds and arytenoid soft tissue Occurs mostly in winters Peak incidence :- 1 – 6 years Male affected more bacterial infection (Hemophilus influenza type b) Concomitant bacteremia, pneumonia, otitis media, arthritis and other invasive infections caused by H.influenza type b may be present ACUTE EPIGLOTTITIS
- 21. Clinical features High fever, sore throat, dyspnea, rapidly progressing respiratory obstruction Patient may become toxic, difficult swallowing, laboured breathing, drooling, hyperextended neck Tripod position (sitting upright and leaning forward) Cyanosis , coma, death Stridor is a late finding ACUTE EPIGLOTTITIS
- 22. Do notexamine the throat Assessment of severity Degree of stridor Respiratory rate Heart rate Level of consciousness Pulse oximetry EXAMINATION
- 23. DIAGNOSIS: “CHERRYRED”APPEARANCE OF EPIGLOTTIS ON LARYNGOSCOPY THUMB SIGN ON LATERAL NECK RADIOGRAPH ACUTE EPIGLOTTITIS
- 24.
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- 26.
- 27. NEED TOBE MANAGED IN ICU WITH ENDOTRACHEAL INTUBATION HELP FROM ANAESTHETIST AND ENT SURGEON BLOOD CULTURES FLUID AND ELECTROLYTE SUPPORT INTRAVENOUS AMPLICILLIN 100 mg/kg/day OR CEFTRIAXONE 100 mg/kg/day . OTHER OPTIONS (CEFUROXIME OR CEFOTAXIME) TOTAL TREATMENT :-7-10 DAYS CHOLRAMPHENICOL 50-75 mg/kg/day IV RIFAMPICIN PROPHYLAXIS TO CLOSE CONTACTS TREATMENT (ACUTE EPIGLOTTITIS)
- 28. VIRAL INFECTIONLEADING TO MUCOSAL INFLAMMATION OF THE GLOTTIC AND SUBGLOTTIC REGIONS COMMONLY DUE TO INFLUENZA (TYPE A), PARAINFLUENZA(1, 2, 3) AND RSV AGE :- 6 MONTHS – 6 YEARS ACUTE LARYNGOTRACHEOBRONCHITIS (VIRAL CROUP)
- 29. CLINICAL FEATURES INITIAL :- RHINORRHEA, MILD COUGH, FEVER(LOW GRADE) LATER (24-48 HOURS) :- BARKING COUGH HOARSENESS OF VOICE NOISY BREATHING (MAINLY ON INSPIRATION) SYMPTOMS WORSEN AT NIGHT AND ON LYING DOWN CHILDREN PREFER TO BE HELD UPRIGHT OR SIT IN BED SYMPTOMS RESOLVE WITHIN A WEEK ACUTE LTB
- 30. CLINICAL EXAMINATION HOARSE VOICE NORMAL TO MODERATELY INFLAMMED PHARYNX SLIGHTLY INCREASED RESP RATE WITH PROLONGED INSPIRATION AND INSPIRATORY STRIDOR ACUTE LTB
- 31. DIAGNOSIS MAINLYA CLINICAL DIAGNOSIS RADIOGRAPH NECK :- STEEPLE SIGN (UNRELIABLE) ACUTE LTB
- 32.
- 33. TREATMENT MOISTOR HUMIDIFIED AIR STEROIDS REDUCE THE SEVERITY AND DURATION / NEED FOR ENDOTRACHEAL INTUBATION PREDNISOLONE PO 2mg/kg/day FOR 3 DAYS NEBULIZED BUDESONIDE 2mg STAT NEBULIZED ADRENALINE (EPINEPHRINE) ACUTE LTB
- 34. Tonsillitis isa viral or bacterial infection in the throat that causes inflammation of the tonsils. Tonsils are small glands (lymphoid tissue) in the pharyngeal cavity. In the first six months of life tonsils provide a useful defense against infections. Tonsillitis is one of the most common ailments in pre-school children, but it can also occur at any age. Children are most often affected from around the age of three or four, when they start nursery or school and come into contact with many new infections. A child may have tonsillitis if he/she has a sore throat, a fever and is off food. Tonsillitis
- 35. Tonsillitis Palatine tonsils (Visibleduring oral examination)
- 36. Tonsillitis iscaused by a variety of contagious viral and bacterial infections. It is spread by close contact with other individuals and occurs more during winter periods. The most common bacterium causing tonsillitis is streptococcus. Causes of tonsilitis
- 37. Encourage bedrest. Introduce soft liquid diet according to the child's preferences. Provide cool mist atmosphere to keep the mucous membranes moist during periods of mouth breathing. Warm saline gargles & paracetamol are useful to promote comfort. If antibiotics are prescribed, counsel the child's parents regarding the necessity of completing the treatment period Advice and treatment:
- 38. The controversyof tonsillectomy: Surgical removal of chronic tonsillitis (tonsillectomy) is controversial. Generally, tonsils should not removed before 3 or 4 yrs of age, because of the problem of excessive blood loss & the possibility of re-growth or hypertrophy of lymphoid tissue, in young children. Management:
- 39. Community acquiredbacterial sinusitis S.pneumoniae H. influenzae S. pyogenes Nosocomial sinusitis Seen in critically ill, mechanically ventilated S. aureus Pseudomonas aeruginosa Serratia marcescens fungal Sinusitis
- 42. Clinical features Sneezing Nasal discharge Facial pressure Fever Purulent drainage Headache Sinus imaging not routinely recommended Clinical features
- 43. Maxillary: usually uncomplicated Ethmoid:cavernous sinus thrombosis-serious Frontal: osteomyelitis of frontal bone; cavernous sinus thrombosis; epidural, subdural, or intracerebral abscess; orbital extension Sphenoid: Rare; extension to internal carotid artery, cavernous sinuses, pituitary, optic nerves; common misdiagnoses include ophthalmic migraine, aseptic meningitis, trigeminal neuralgia, cavernous sinus thrombosis Acute sinusitis: complications
- 44. Otitis externa Acute,localized: often S. aureus, S. epidermidis or S. pyogenes Acute diffuse (swimmer’s ear): gram-negative rods, especially Ps. Aeruginosa ; Rx: topical quinolones Chronic: mainly with chronic otitis media Malignant: life-threatening infection in diabetics, elderly, immunecom promised
- 45. S. pneumoniae andH. influenzae the leading causes in all age groups (most H. flu is from non-typable strains and not “B”) Moraxella catarrhalis: 10% of cases Some cases may be viral (RSV, influenza, enteroviruses) Mycoplasma pneumoniae: inflammation of the tympanic membrane (“bullous myringitis”) Acute otitis media
- 46. Acute otitis media Critical role of eustachian tube as conduit between nasopharynx, middle ear, and mastoid air cells Children have shorter, wider eustachian tubes than adults
- 47. Presence offluid in the middle ear AND Ear pain, drainage, hearing loss The fluid may take weeks to resolve Amoxicillin remains the drug of choice Beta-lactamase producing strains of H. influenza will need amoxicillin/clavulanic acid or cephalosporins Diagnosis and treatment
- 48.
- 49. Inflammatory syndromeof the pharynx Most cases are viral Most important bacterial cause is Streptococcus pyogenes (15-20%) Presents with sore or scratchy throat In severe bacterial cases there may be odynophagia, fever, headache Acute pharyngitis
- 50. Viral: edemaand hyperemia of tonsils and pharyngeal mucosa Streptococcal: exudate and hemorrhage involving tonsils and pharyngeal walls Epstein-Barr virus (infectious mono): may also cause exudate, with nasopharyngeal lymphoid hyperplasia Acute pharyngitis: physical examination
- 51. Adenoviral pharyngitis Pharyngeal erythemaand exudate may mimic streptococcal pharyngitis Conjunctivitis (follicular) present in 1/3 to 1/2 of cases; commonly unilateral but bilateral in 1/4 of cases Pharyngoconjuntival fever
- 52. Herpangina Uncommon Due to coxsackieviruss Small, 1-2 mm vesicles on the soft palate, uvula, and anterior tonsillar pillars which rupture to form small white ulcers Occurs mainly in children Also think of Herpes simplex virus when you see vesicular lesions Vesicular lesions
- 53. Vincent’s angina:anaerobic pharyngitis (exudate; foul odor to breath) Ludwig’s angina- cellulitis of dental origin Quinsy: peritonsillitis/peritonsillar abscess. Medial displacement of the tonsil; often spread of infection to carotid sheath Vincent’s angina and Quinsy
- 55. Classic diphtheria(Corynebacterium diphtheriae): slow onset, then marked toxicity Arcanobacterium hemolyticum (formerly Cornyebacterium hemolyticum): exudative pharyngitis in adolescents and young adults with diffuse, sometimes pruritic maculopapular rash on trunk and extremities Diphtheria
- 56. Diphtheria fibrous pseudomembrane withnecrotic epithelium and leukocytes
- 57. Symptomatic Penicillinfor Strep throat Macrolides for pen allergic patients Add an anti-anaerobic agent for Vincent’s and Ludwig’s angina Treatment
- 58. BRONCHITIS/BRONCHIOLITIS PNEUMONIA LOWERRESPIRATORY TRACT INFECTIONS
- 59. Inflammatory diseaseof the bronchioles Peak age of onset : 6 months Most common agent :- rsv Male : female :- 2:1 Occurs mostly in winter/spring BRONCHIOLITIS
- 60. Coryza withcough followed by worsening breathlessness Vomiting Irritability Wheeze Feeding difficulty Episodes of apnoea CLINICAL FEATURES
- 61. Rapid shallowbreathing (60-80/min) Cyanosis / pallor Flaring of alae nasi Use of accessory muscles of respiration Subcostal /intercostal recessions Expiratory wheeze / grunting Prolonged expiration Hyper-resonant percussion notes Chest hyperinflation Liver/spleen palpable Bronchiolitis obliterans EXAMINATION FINDINGS IN BRONCHIOLITIS
- 62. DIAGNOSIS ChestX-ray Hyperinflation, increased lucency and increased bronchovascular markings and mild infiltrates Pulse oximetry Nasopharyngeal swabs (viral culture) Viral antibody titers (iat for rsv) BRONCHIOLITIS
- 63. A chest X-raydemonstrating lung hyperinflation with a flattened diaphragm and bilateral atelectasis in the right apical and left basal regions in a 16-day-old infant with severe bronchiolitis
- 64. COMPLICATIONS Pneumonia Pneumothorax Dehydration Respiratory acidosis Respiratory failure Heart failure Prolonged apneic spells death BRONCHIOLITIS
- 65. TREATMENT Mainlysupportive Prop up (30 – 40 degrees) Oxygen inhalation (achieve o2 >92%) If tachypneic, limit the oral feeds and use a ng tube for feeding Parenteral fluids to limit dehydration Correct resp acidosis and electrolyte imbalance Bronchodilators for wheeze (nebulized adrenaline) Mechanical ventilation (severe resp distress or apnoea) BRONCHIOLITIS
- 66. Inflammation ofthe lung parenchyma and is associated with the consolidation of the alveolar spaces Developed world Viral infections Low morbidity and mortality Š Developing world Common cause of death Bacteria and PCP in 65% Š ARI case management WHO 84% reduction in mortality Respiratory rate, recession, ability to drink Cheap, oral and effective antibiotics, Co-trimoxazole, amoxycillin Maternal education Referral PNEUMONIA
- 67. Š Varyaccording to Age, immune status, where contracted Š Community acquired (CAP) Developing countries S. pneumoniae, H. influenzae, S aureus Viruses 40% Other: Mycoplasma, Chlamydia, Moraxella Developed countries Viruses: RSV, Adenovirus, Parainfluenza, Influenza Mycoplasma pneumoniae and Chlamydia pneumoniae Bacteria: 5-10% Etiology
- 68. ETIOLOGY ACCORDING TOAGE AGE GROUP CAUSATIVE ORGANISM NEONATES GROUP B STREPTOCOCCUS E.COLI KLEBSIELLA STAPH AUREUS INFANTS PNEUMOCOCCUS CHLAMYDIA RSV H.INFLUENZA TYPE b CHILDREN 1 TO 5 YRS RESPIRATORY VIRUSES PNEUMOCOCCUS H.INFLUENZA TYPE b C.TRACHOMATIS M.PNEUMONIAE S.AUREUS GP A STREPTOCOCCUS CHILDREN 5 TO 18 YRS M.PNEUMONIAE PNEUMOCOCCUS C.PNEUMONIAE H.INFLUENZA TYPE b
- 69. WHO Classification andmanagement NO PNEUMONIA COUGH NO TACHYPNEA -HOME CARE -SOOTHE THE THROAT AND RELIEVE COUGH -ADVISE MOTHER WHEN TO RETURN -FOLLOWUP IN 5 DAYS IF NOT IMPROVING PNEUMONIA -COUGH -TACHYPNEA -NO RIB OR STERNAL RETRACTION -ABLE TO DRINK - NO CYANOSIS -HOME CARE -ANTIBIOTICS FOR 5 DAYS -SOOTHE THE THROAT AND RELIEVE COUGH -ADVISE MOTHER WHEN TO RETURN -FOLLOWUP IN 2 DAYS SEVERE PNEUMONIA -COUGH -TACHYPNEA -RIB AND STERNAL RETRACTION -ABLE TO DRINK -NO CYANOSIS -ADMIT IN HOSPITAL -GIVE RECOMMENDED ANTIBIOTICS -MANAGE AIRWAY -TREAT FEVER IF PRESENT VERY SEVERE PNEUMONIA -COUGH -TACHYPNOEA -CHEST WALL RETRACTION -UNABLE TO DRINK -CENTRAL CYANOSIS -ADMIT IN HOSPITAL -GIVE RECOMMENDED ANTIBIOTICS -OXYGEN -MANAGE AIRWAY -TREAT FEVER IF PRESENT
- 70. Significant riskfactors are younger age (2-6 months), low parental education, smoking at home, prematurity, low birth weight, weaning from breast milk at < 6 months, a negative history of diphtheria, pertussis and tetanus vaccination, anaemia, malnutrition and overcrowding. Infection rate higher in siblings of school children who introduce infection in the household. Other risk factors Congenital lung cysts Chronic lung disease Immunodeficiency Cystic fibrosis Sickle cell disease Tracheostomy in situ HIGH RISK CHILDREN FOR PNEUMONIA
- 71. Š Signof respiratory distress; nasal flaring & chest indrawing Younger than 2 months Decreased level of consciousness Stridor when calm Severe malnutrition Associated symptomatic HIV/AIDS Danger Signs (IMCI)
- 72. SIGNS OF RESPIRATORYDISTRESS
- 73. SIGNS OF RESPIRATORYDISTRESS
- 74. Bacterial – Poorly demarcated alveolaropacities with air bronchograms – Lobar or segmental opacification Radiology
- 75.
- 76. Š Cluesto other specific organisms Staphylococcus – areas of break-down Klebsiella, anaerobes, H. influenza or TB –cavitating or expansile pneumonia TB, S. aureus, H. influenza pleural effusion and empyema Radiology
- 77. White cellcount and CRP >15,000 – 40,000/mm3 neutrophil predominance Blood cultures 25% positive NASOPHARYNGEAL ASPIRATE Viral immunoflorescence in infants Sputum specimen Gram staining Acid fast bacilli Pleural fluid examination (if present) ASO titer (in case of streptococcal pneumonia) Tuberculin skin test Viral Titres culture antigen Diagnosis
- 78. Empyema Lungabscess Pneumothorax Pneumatocele Pleural effusion Delayed resolution Respiratory failure Metastatic septic lesions Meningitis Otitis media Sinusitis Speticaemia COMPLICATIONS OF PNEUMONIA
- 79. Š Antibiotics Under 5 yrs First line treatment :- amoxicillin Alternatives : coamoxiclav, cefaclor,(for typical) macrolides (for atypical) Over 5 yrs First line treatment :- amoxicillin or macrolides Alternatives :- macrolide or flucloxacillin + amoxicillin Severe pneumonia Co-amoxiclav, cefotaxime or cefuroxime Special categories (as per the suspected organism) Treatment
- 80. Treatment in specialgroups GROUP ORGANISMS ANTIBIOTICS IMMUNOCOMPROMISED -GRAM NEGATIVE -S. AUREUS -OPPORTUNISTIC PNEUMOCYSTIS JIROVECI -M. TUBERCULOSIS AMPICILLIN + CLOXACILLIN + AMINOGLYCOSIDE LESS THAN 3 MONTHS -GRAM NEGATIVE -GROUP B STREPTOCOCCUS -S.AUREUS AMPICILLIN + AMINOGLYCOSIDE HOSPITAL ACQUIRED PNEUMONIA -GRAM NEGATIVE -METHICILLIN RESISTANT S. AUREUS AMINOGLYCOSIDE + VANCOMYCIN + CEPHALOSPORIN (3RD GENERATION)
- 81. Š Oxygen intranasaly Š Hydration 50 – 80ml/kg/day Š Temperature control Š Airway obstruction management Chest drain :- for fluid or pus collection in chest (empyema) Treatment (contd.)
- 82. Š Mostchildren recover without residual damage Š Incorrect treatment leads to tissue destruction and bronchiectasis Š Half of children with pneumonia secondary to measles or adenovirus have persistent airway obstruction Prognosis
- 83. Early diagnosis ofpneumonia and the warning signs of severe disease and prompt management – key factors which determine the outcome of disease Guidelines have been given by WHO regarding management and use of antibiotics. Recent changes – Management as per the IMNCI protocol PREVENTION AND CONTROL OF ARIs
- 84. as per the“Integrated Management of Neonate & Child Illnesses” (IMNCI) protocol
- 85. History takingand clinical assessment very important Age of the child, for how long the child has been coughing, whether the child is able to drink, has the young infant stopped feeding well, does the child have fever, is the child drowsy or difficult to wake, did the child have convulsions, is there irregular breathing, any history of treatment. Clinical Assessment
- 86. 1. COUNTING THENUMBER OF BREATHS IN ONE MINUTE - to assess fast breathing Respiratory rate cut-offs: >/= 60 breaths per minute in a child less than 2 months >/=50 breaths per minute in child aged 2month upto 12 months >/=40 breaths per minute in child aged 12 months upto 5 years Physical examination
- 87. 2. LOOK FORCHEST INDRAWING when the child breathes IN 3. LOOK AND LISTEN FOR STRIDOR when the child breathes IN 4. LOOK FOR WHEEZE when the child breathes out 5. FEEL FEVER OR LOW BODY TEMPERATURE 6. CHECK FOR SEVERE MALNUTRITION 7. CHECK FOR CYANOSIS Physical examination cont.
- 88. CHILD BELOW2 MONTHS Very severe disease Severe pneumonia No pneumonia CHILD AGED 2 MONTHS UPTO 5 YEARS Very severe disease Severe pneumonia Pneumonia No pneumonia (cold & cough) CLASSIFICATION OF DISEASE
- 89. SIGNS STOPPED FEEDING WELL CONVULSIONS ABN. SLEEPY STIDOR IN CALM CHILD WHEEZE FEVER/LOW BODY TEMP. SEVERE CHEST IDRAWING FAST BREATHING NO SEVERE CHEST INDRAWING NO FAST BREATHING CLASSIFY AS VERY SEVERE DISEASE SEVERE PNEUMONIA NO PNEUMONIA TREATMENT REFER URGENTLY KEEP WARM GIVE FIRST DOSE OF ANTIBIOTIC REFER URGENTLY KEEP WARM GIVE FIRST DOSE OF ANTIBIOTIC ADVICE FOR HOME CARE EXPLAIN DANGER SIGNS MANAGEMENT OF ARI CHILDREN BELOW 2 MONTHS
- 90. MANAGEMENT OF ARI CHILDAGED 2 MONTHS UPTO 5 YEARS SIGNS NOT ABLE TO DRINK CONVULSIONS ABNORMALLY SLEEPY OR DIFFICULT TO WAKE STRIDOR IN A CALM CHILD SEVERE MALNUTRITION FAST BREATHING CHEST INDRAWING NASALFLARI NG GRUNTING FAST BREATHING ONLY NO CHEST INDRAWING NO FAST BREATHING NO CHEST INDRAWING CLASSIFY AS VERY SEVERE DISEASE SEVERE PNEUMONIA PNEUMONIA NO PNEUMONIA/ COLD & COUGH TREATMENT REFER URGENTLY GIVE FIRST DOSE OF ANTIBIOTIC TREAT FEVER, IF PRESENT TREAT WHEEZE, IF PRESENT REFER URGENTLY GIVE FIRST DOSE OF ANTIBOTIC TREAT FEVER TREAT WHEEZE ADVICE FOR HOME CARE GIVE ANTIBIOTIC TREAT FEVER TREAT WHEEZE ASSESS AND TREAT EAR PROBLEM/ SORE THROAT TREAT FEVER TREAT WHEEZE
- 91. Parenteral – BenzylPenicillin or Ampicillin & Gentamycin Oral – Cotrimoxazole tablets / suspension Antibiotics recommended
- 92. MEASLES HIBVACCINE PNEUMOCOCCAL PNEUMONIA VACCINATION
- 93.